ACSL3/GABARAPL2 Ameliorates Vascular Endothelial Cell Aging and Injury Through Protective Autophagy to Alleviate Ferroptosis.

Hong-Fei Sang, Lin-Lin Wan, Chuang Zhang, Xin-Qing Li, Jie Pan, Peng Miao, Feng-Rui Lei

Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China. · pubmed

Paper

Abstract

Vascular endothelial cell (VEC) dysfunction is a key contributor to vascular diseases. Oxidative stress-induced ferroptosis accelerates VEC aging and injury, while protective autophagy mitigates this damage by clearing damaged organelles and reducing oxidative stress. GABARAPL2, a critical autophagy-related protein, and ACSL3, a regulator of lipid metabolism and ferroptosis, are emerging as interconnected mediators of cellular protection. However, their precise roles in oxidative stress-induced VEC aging and injury remain unclear. This study aimed to investigate how GABARAPL2 and ACSL3 regulate autophagy and ferroptosis to protect VECs. Human umbilical vein endothelial cells (HUVECs) were treated with hydrogen peroxide to establish a cellular oxidative stress model. Gene expression was analyzed through Western blot and immunofluorescence, while cell viability, apoptosis, reactive oxygen species (ROS), Fe

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Research summary

The paper claims that GABARAPL2 and ACSL3 regulate autophagy and ferroptosis to protect vascular endothelial cells from oxidative stress-induced aging and injury. This research addresses mechanisms that contribute to cellular aging and dysfunction, which are central to understanding and potentially mitigating age-related diseases.

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